Category Archives: Drugs

Smoking CBD Hemp May Ease Your Arthritis Pain

Arthritis is one of the many “silent” ailments affecting the nation. While you don’t hear as much about arthritis as you do other headline-grabbing conditions, the truth is that over 20 million people suffer with severe, debilitating arthritis pain every single day. Luckily, CBD hemp may be the answer.

Arthritis is also a condition that is not well understood by most people. Arthritis can be much more than simply “joint pain.” There are actually over 100 different types of arthritis, and while some may cause local discomfort in the fingers, others can also cause a number of other serious symptoms: sensitivity and pain throughout the entire body, sciatica that makes normal activity difficult, even depression and low energy.

Moreover, there is no “cure” for most forms of arthritis. Nor are all forms fully understood. Those diagnosed with the condition must therefore, instead, consider ways to manage the pain and maintain an acceptable quality of life.

CBD hemp might provide an answer.

What is CBD Hemp and How Does it Treat Arthritis Pain?

CBD is a cannabinoid that comes from the hemp plant. While it can be extracted from cannabis, it is NOT psychoactive like THC and will not cause a person to get “high”.

What CBD can do however, is to treat both inflammation AND pain. It does this by binding to a network of cell receptors called the endocannabinoid system. These cells are responsible for controlling such things as mood, memory, immune function, appetite, sleep, and pain.

Seeing as many forms of arthritis are autoimmune conditions – meaning that the body is attacking itself (thus leading to inflammation/swelling) – CBD appears to be beneficial in reducing that swelling. What’s more, is that CBD can help to improve the mood AND reduce the experience of the pain.

For these reasons, more and more people are now using CBD-based products to manage arthritis symptoms – with extremely promising results.

Why Smoke CBD?

While CBD hemp can be taken in many forms, oral use (using a pill) is not the most effective for treating your arthritis. This is because orally ingested CBD has low “bioavailability.” This means that while you might have consumed a certain amount of CBD, only a small portion of that will be usable by your body.

In other words, are you actually benefiting from the CBD that you’re taking? That’s a pretty significant question. If you’re swallowing a pill and only getting 10% of the dose effectively, then you’re throwing money down the drain. Most importantly, you’re not getting the effects, which you may need to function more normally.

Sublingual actually means beneath the tongue and this is one way that you can use any orally ingested psychoactive compound. By placing the pill beneath your tongue, it will actually dissolve more quickly and enter the blood stream. But while sublingual administration is preferable to simply swallowing, the fact still remains that pills won’t be as potent as vaping or smoking.

Another issue with using any pill form of drug is that you are introducing more chemicals and ingredients into your system. Pills need binding agents and coatings and in some rare cases, these can cause allergic reactions. And while marijuana use is now legal in California, it’s still possible that you might have acquired the substance from a less well-regulated source (shall we say…) – meaning that there’s a high chance it may have been contaminated or even cut with other things. Apart from anything else, smoking CBD hemp cigarettes and vaping CBD hemp are definitely more hygienic!

No smoke without fire – the link between smoking and mental health

A recent study suggested a causal association between smoking tobacco and developing psychosis or schizophrenia, building on research about the relationship between the use of substances and the risk of psychosis. While cannabis is one of the usual suspects, a potential link with tobacco will have come as a surprise to many.

The report was based on a review of 61 observational studies and began with the hypothesis that if tobacco smoking played a part in increasing psychosis risk, rather than being used to deal with symptoms that were already there, people would have higher rates of smoking at the start of their illness. It also posited that smokers have a higher risk of developing psychosis and an earlier onset of symptoms to non-smokers. They found that more than half of people with a first episode of schizophrenia were already smokers, three times higher than that of a control group.

However, one of the limitations of the study, as the authors admit, is that many of the studies in their review did not control for the consumption of substances other than tobacco, such as cannabis. As many people combine tobacco with cannabis when they smoke a joint, the extent to which tobacco is the risk factor is still unclear.

One clear message the research highlighted was the high level of smoking among those with mental health problems and that smoking is not necessarily simply something that alleviates symptoms – the so-called “self-medication hypothesis”.

Almost half of all cigarettes

The figure is stark: 42% of all cigarettes smoked in England are consumed by people with mental health problems. So while the life expectancy of the general population continues to climb, those with a severe mental health problem have their lives cut short by up to 30 years – in part due to smoking.

Since the 1950s, rates of smoking have dramatically reduced in the population while the number of people with psychosis has remained constant. So why has the incidence of psychosis not mirrored the reduction in the overall numbers of smokers? Two factors might explain this. First institutional neglect has held up efforts and resources employed to reduce smoking for people with mental health problems – until recently public health campaigns have ignored this group with justifications that “surely they have enough to worry about without nagging about smoking” or “it’s one of the few pleasures they have”.

A more sinister role is also played by the tobacco industry, who have not been passive or unaware of one of their most loyal consumer groups: people with mental health problems. The industry has been active in funding research that supports the self-medication hypothesis, pushing the idea that people with psychosis need tobacco to relieve their symptoms, rather than tobacco having any link to those symptoms. The industry has also been a key player in obstructing hospital smoking bans which they perceive as a threat to tobacco consumption. Worse still they have marketed cigarettes specifically to people with mental health problems.

Combining substances

Time to quit.
Smoking by Shutterstock

People with psychosis use substances for the same reasons you and I do: relax or feel less stressed. And the good news is, counter to many people’s preconceptions, individuals with mental health problems are no different to anyone else in their desire and ability to quit smoking.

This is welcome given the clear links between smoking and physical health. But there are particular issues when it comes to smoking and those with psychosis. For example, smoking impacts on the medical treatment of psychosis, as tobacco is known to interact with Clozapine, one of the drugs used to treat the condition. Because smoking interferes with the therapeutic action of Clozapine and some other anti-psychotics, requiring higher doses of the drug.

Then there’s the cannabis question. People with mental health problems are more likely to use drugs such as cannabis. This is usually combined with tobacco when smoked in a joint. So initiation into cannabis and its continued use contributes to higher rates of tobacco dependence for people with mental health problems.

The relationship between cannabis and psychosis has preoccupied researchers, policy makers and clinicians for decades. Unfortunately most of this evidence which has influenced and underpinned public health messages about cannabis is either outdated or methodologically flawed.

Since many of the seminal studies on this issue were carried out, there has been a marked change in the type of cannabis that is available. These studies were recruiting and investigating users who were exposed to lower potency varieties of cannabis. Over the past decade, higher potency forms of cannabis such as “skunk” have become dominant on the streets. This has been compounded by research being done by simply enquiring whether research participants currently use or have ever used cannabis. This assumes cannabis is a single type of drug, rather than a range of substances with varying strengths and constituent ingredients. To make matters worse, we rely on proxy measures of cannabis potency drawn from seizures made by the police. Such seizures may not be representative of contemporary cannabis availability.

Many people are exposed to a combination of drugs, whether prescribed, recreational or a mix of both. This raises the potential for interactions, where the effect of one drug alters the effects of another. This raises a further possibility in the smoking, cannabis and psychosis story. Could some people’s psychosis be attributed to an interaction between cannabis and tobacco? Information about drug interactions is scarce and pharmaceutical research has routinely excluded people who use substances from drug trials. This does not reflect reality as many people will combine medication with recreational drug use.

All of these factors serve as a useful reminder how little we know about the causes of psychosis, the role drugs play and the many vested interests that direct the route we take in trying to understand how we can prevent or treat people who are affected by mental health problems.

The Conversation

Ian Hamilton is Lecturer in Mental Health at University of York.

This article was originally published on The Conversation.
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The pill – it’s safer than driving to work

A study published in The BMJ today suggests a link between newer contraceptive pills and higher risk of serious blood clots. The finding is not new, but it may be cause for a different kind of concern.

During their fertile years, between three and five women of every 10,000 who are not pregnant and not taking the pill are likely to develop blood clots every year. The research published today found older contraceptive pills double this “background” risk of blood clots, and the newer pills have roughly doubled the risk again.

Several studies published over the past 20 years show very similar findings. What this research brings to the table are larger numbers of women and more careful attention to factors in their medical history that could potentially skew the results.

It’s likely the media will pounce on this story; there will be testimonies from women who have experienced blood clots while taking the pill and a plethora of personal injury lawyers spruiking their business. Women across the world will be scared into stopping their contraception until it all blows over. I know this because I’ve seen it before, and I think that’s what we should be concerned about.

Back and forth

We’ve known the pill increases a woman’s risk of blood clots and stroke since it was first marketed. By the 1990s, concern had been tempered by the fact that this risk was greatly reduced by pills containing only a quarter of the oestrogen compared to the 1960s. The development of several newer progestogens in the 1980s had also increased the range of pills available, making it more likely that most women could find a combination that suited them.

But then, in 1995, three studies published in The Lancet suggested pills containing these newer progestogens posed twice the risk of blood clots as the older ones, just as the study published today does. Frenzied media coverage of the finding led many women to simply discontinue their contraception.

As a result, 1995-96 saw a 9% increase in abortion rates in Britain as well as a 25% increase in births. And both pregnancy and birth hold significantly higher risks of blood clots than any contraceptive pill, with rates at least ten times higher.

Within a few years, the controversy settled down somewhat when a number of epidemiologists pointed out that doubling an extremely small risk has no significant public health impact. But then, between 2007 and 2014, it all started again when a number of studies reached conflicting conclusions about whether there were any real differences in clotting rates between various pills.

Every woman considering using the contraceptive pill should discuss the risks it poses to her health as well as available alternatives with her prescribing doctor.
Annabelle Shemer/Flickr, CC BY-NC-ND

Two very large studies that kept track of women from the time they started various pills showed no difference in blood-clotting risk between any of the pills the women were taking. But research like this is extremely expensive and only within the funding reach of either governments or pharmaceutical companies. In this case, it was the latter. Despite the fact that both studies were independently monitored, they were attacked as having commercial bias.

Four out of six of the remaining studies, which used various databases to look back from a blood clot diagnosis and capture the kind of pill the woman was taking, suggested the newer pills doubled risk. But the inevitable lack of “real-time” information in this kind of research also leaves it open to many potential biases.

The just-published BMJ study provides further evidence for research showing increased risk, and its publication will no doubt re-ignite the debate about the safety of newer contraceptive pills. It’s clearly time for an appraisal of the actual risks involved.

Being cautious

Even if we were to adopt the worst-case scenario from all the studies published to date, being on one of the older versions of the contraceptive pill increases the risk of blood clot from three and five per 10,000 women each year to somewhere between five and eight. Taking one of the newer ones raises it to between nine and 14.

So although a doubling of clotting risk sounds alarming, it actually translates to an additional four to six cases per 10,000 users of the newer pills a year.

It’s also important to recognise that only one in 100 women who have a blood clot will die from it. That risk of death could be cancelled out statistically by driving for two fewer hours each year. Put another way, the risk of a woman dying from a road accident is approximately 25 times that of death from a pill-related clot.

This is not to say we should be blasé about the risks posed by the contraceptive pill. It is above all a medication, which means some of its benefits may be compromised by – potentially serious – side effects. Every woman considering using the contraceptive pill should discuss the risks it poses to her health as well as available alternatives with her prescribing doctor.

This study adds to what is known about blood clot risk on various oral contraceptive pills, but it doesn’t claim to provide the definitive answer. I hope that, as we again debate the risks posed by the pill, we don’t lose sight of the fact that, for most women, the benefits of combined contraceptives far outweigh risks.

The Conversation

Terri Foran is Lecturer in the School of Women’s and Children’s Health at UNSW Australia.

This article was originally published on The Conversation.
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biomimicry and the search for new tech

Biomimicry is the study of nature as inspiration for human designs in effort to fit  human technology into a more efficient and workable, sustainable model. Each organism alive today has the potential to teach humankind about the systems and rules it follows. Natural solutions aren’t just about having better materials.

They are about making products that might empower mankind against dwindling resources. Ecosystems aren’t just where we all live and consume resources but they are a resource of information as well. The ecosystem is self-replenishing and efficient and can be channeled and worked with in a way that has yet to be attempted. Potential new materials come with  side effects that warrant equal consideration. Biomimicry is a paradigm that fits many emerging techs. Take a look at spider venom’s effect on the drug industry, for example:

A peptide found in spider venom might lead to a safer class of painkillers. What other drugs, chemicals and designs are being inspired by biology and newly-studied species?

Biomimicry is a relatively young term, describing designs that derive inspiration by emulation of designs found in nature. The movement is focused on sustainable human endeavors and projects that will compliment the environment humans share with the rest of the natural world and thus better humanity’s chance for survival. Check out this video, the most recent by Janine Benyus, one of the idea’s most vocal proponents.

You might wonder why these chemicals are found in nature at all? There are many functions and motivations behind the diverse, unfound substances found in the Eco-system. Plants develop poison to discourage predators. some develop drugs to encourage other species to assist with seed dispersal. Evolution has provided the earth with highly diversified species of plants fungi and animals the vast majority of which have yet to be explored.

French researchers discovered a painkiller as powerful as morphine in the venom of e infamous African black mamba snake. Then there is a potential psoriasis treatment derived from the venom of the Caribbean sun anemone, undergoing testing in the U.S. might help sufferers with psoriasis, autoimmune disorders, multiple sclerosis and rheumatoid arthritis.gecko

Textures and surface patterns of geckos have been studied for stickiness. Skin textures of some animals have been proven to possess antimicrobial properties, in that bacterial colonies can’t find a way to attach to surfaces, making water currents and frequent rinsing enough to eliminate infective agents.

Artificial limb design and development has been greatly advanced by designs mimicking the weight-bearing capacity of other animals. New technologies are being developed to grant disabled people the ability to feel touch, as the natural mechanisms controlling pain, touch and movement are further understood.


In recent biomimetic news, we may see a mastery of understanding the human eye lead to a leap in ocular and immersive tech. MHOX is an Italian design firm who would like  synthetic replacement eyes.EYE to become an affordable, regular upgrade people opt for. Their work could restore sight to the blind and be the missing link to allow locative tech and a lot of web 2.0 concepts to become workable mainstream realities.

There is an initial shock in some people when these concepts are explained. Something about the current trends over the last few decades favoring straight, clean lines that are inspired by lifeless geometry over bio-inspired,  flowing shapes.

The drugs and prosthetics discussed, theorized and predicted in the biomimetics industries doesn’t have to turn humans into cyborgs, although some proponents wouldn’t be against that. It is likely that the public will be more inclined to accept these advancements as they are developed. Decades back people might have been less receptive to plastic hip replacements and artificial hearts, but the medical community has become very good at installing these prosthetics as minimally invasive, outpatient procedures.


Jonathan Howard
Jonathan is a freelance writer living in Brooklyn, NY

Spider Venom and the Search for Safer Pain Meds

Some of the most poisonous animals on the planet are found down under. Australian researchers retrieved exciting new data when taking a closer look at spider venom. Biosynthesized chemicals designed to be highly reactive with other organisms could inspire new drugs and, eventually, an entire new class of painkillers.

It can be defensive but the function of spider venom is often to incapacitate or kill prey. University of Queensland academics released their findings in The British Journal of Pharmacology, after they isolated seven unique peptides found in certain spider venoms that can block the molecules that allow pain-sensitive nerve pathways to communicate with the brain. One of the pepetides originated in the physiology of a Borneo orange-fringed tarantula. That peptide possessed the correct chemical structure, combined with a stability and effectiveness to become a non-opiate painkiller.

15% of all adults are in chronic pain, according a study published in 2012 Journal of Pain. Most readers are already aware of the danger of addiction and lagging effetiveness of opiate drugs like morphine, hydrocodone, oxycodone. The medical community is hungry for a change in available medications. Opiates are all derivatives or inspired by opium plants which have been tried and tested for centuries. Venomous spiders are difficult to study but the motivation for new drugs has loosened funding with the help of promising finds like this one.

“Spider venom acts in a different way to standard painkillers,” ~ Dr. Jennifer Smith, research officer @ University of Queensland’s Institute for Molecular Bioscience.

While cessation from pain might in itself create an addictive reaction, this venom is promising, according to Dr. Smith, because it blocks the channel through which the pain would even reach the brain. Opiates merely block the widespread opioid receptors in actual brain cells, deep within and in the surrounding nerve tissue of the brain itself.

What’s the mechanism of action for this spider-drug? Some people are born with a rare genetic defect that renders them unable to feel pain. Geneticists identified the human gene responsible, known as SCN9A. Dr. Smith hopes the peptide will enable the cells of a human without the defect to shut down part of the DNA that manifests this immunity to pain.

There could be other breakthroughs in medicine and chemistry. The findings are awesome in the Australian project but those researchers only documented findings of roughly 200 out of 45,000 known species of spider.  Out of those 200, 40% contained peptides that interacted with the way pain channels communicate. The next step would be to test the painkillers on animals.

“We’ve got a massive library of different venoms from different spider species and we’re branching out into other arachnids: scorpions, centipedes and even assassin bugs,” said Dr. Smith.


Jonathan Howard
Jonathan is a freelance writer living in Brooklyn, NY

Steroids Almost Drove One Woman to Suicide

This is the story of Jane. A healthy, stable woman in her twenties who, only weeks after moving from a rural town in Wisconsin landed the job of her dreams in the Big Apple, otherwise known as the city that never sleeps. I mention that, because it runs parallel to Jane’s initial experiences in New York: for the first couple of weeks after her uprooting, Jane wasn’t sleeping either. Not only that, Jane was facing a dangerous depression. A meloncholoy that got worse and worse every day, to the the point she found herself spending her days on the couch, immobile to the point she could not even muster up the emotional strength to answer the phone. It wasn’t long before Jane became suicidal and found herself in a hospital after spending an hour or so on the ledge of her building, ready to jump and end it all.


Of course, the big question here is why. Why would a woman who had already undergone the stress of moving from a little town to the most threatening city of them all and on top of that, land her dream job in a well-known advertising company want to end her life? There is one notable glitch: since the move, Jane had developed asthma, an extrememly common occurence among transplants to an urban environment with poor air quality. After multiple attempts at treating her new breathing ailment with inhalers all of which proved ineffective, her doctor prescribed an oral steroid – et voila! it worked.

But that’s when the weird stuff started happening. Just a week or two after beginning the medication, Jane woke up one morning to a sudden rush of overwhelming and heavy sadness – nothing, she explained, like she had ever encountered before. She could not think of anything that would explain this very sudden and very intense despair. Within a day, the funk got bluer. She sat on the couch and didn’t move, and when it was time to go to bed, she couldn’t sleep and therefore resumed her intitial position on the couch. Jane stopped eating and drinking, cried uncontrollably and remained there in a catatonic state, and by the next day, the suicidal thoughts came creeping in. While the idea was a surprise to normal Jane, to depressed Jane, it seemed awfully alluring and relieving. Depressed Jane won over, and before she knew it, she found herself teeterng on the edge of her window sill deciding whether or not to take the plunge. Thankfully, in a sudden state of terror, Jane pulled herself back into her apartment and called 911.


When confronted with Jane’s story, the doctor in the ER was perplexed. Most suicide attempts, as you can imagine, are usually triggered by traumatic events such as a bad break-up, a death in the family, and so on. But in Jane’s case, just the opposite was true. While Jane’s doctor first thought of bi-polar disorder or some type of mania, the diagnosis didn’t seem to fit her case. Although she descried herself as feeling “euphoric” prior to the depressive episode, the euphoria was mild and not accompanied by the disorganized thoughts and behavior that go hand-in-hand with such a diagnosis. Further, her functioning was normal up to the episode, and she had no history of psychiatric illness at all. Jane was then asked what type of medications she’d been on, to which she replied “none”. She explained that she had been prescribed asthma medication but that she was “done with it”. Because asthma is a chronic condition, Jane’s doctor thought her answer to be a little off the mark. With a little more research including a call to her pharmacy, it was discovered that she had in fact been prescribed a high dose of oral steroids for a week along with a second prescription for a tapering dose of the same medication – but Jane never picked up that second prescription.

The medication that Jane had been prescribed was a corticosteroid, alternately known simply as a steroid. Corticosteroids are very powerful hormones produced by our adrenal glands  and physicians are known to prescribe them as inti-inflammatory drugs, in this case to reduce the inflammation in Jane’s lungs that was happening due to her asthma. Steroids have an array of physiological effects, including regulating the immune system and metabolism. When a person is on steroids, her adrenal glands don’t function as diligently as they would were she not on them. The body recognizes these drugs and in response, cuts back on the amount of steroids it would normally produce. Sometimes, it stops producing these hormones altogether. If a person stops taking these steroids, the adrenal glands will wake up, but this waking up process is sort of like trying to get an adolescent out of bed – it takes time, and sometimes, lots of time. Most high-dose steroids need to be tapered over weeks or months to give the adrenal glands time to “get out of bed” and start functioning again. In the case of Jane, it’s safe to say that when she stopped taking her steroids, her adrenal glands got all wonky and needed way more time than was allowed to wake up.


Steroids are also known to alter mood and behavior, sometimes creating extreme happiness, other times creating severe depression – which is what happened to Jane. These medications are so powerful in fact, that they can even trigger psychosis, extreme anger – and yes, thoughts of suicide. It is more than likely that this is what happened to Jane. She had been on the medication long enough to supress her adrenal glands, and when she stopped taking them, the sudden and severe drop in her blood steroid levels was catastrophic enough to cause her to spiral into a deep dpression that led to suicidal behavior.

Jane was monitored by psychiatrists for a couple of days, and when they restarted her on the steroids, it was like night and day. The depressed, desheveled Jane that had been rolled into the ER after a suicide attempt had transformed into a cheerful (nonetheless unnerved), articulate woman who clearly did not belong on a psychiatric ward. She was discharged within a short period of time, after a slow steroid taper to allow her adrenal glands to start working on their own again.

The story of Jane ends here. It is a not only a clear illustration of how a quick analysis of her symptoms could have led to a misdiagnosis of a primary psychiatric disorder, but a lesson about  the danger of medication when not taken appropriately. There are lots of close calls when it comes to medications and their effects – but this one comes a little too close to the ledge.

Are doctors following best practice when prescribing antipsychotic meds to kids?

There’s been a lot of attention in the media about the number of children taking antipsychotic and other psychiatric medications. The assumption behind most of these stories is that these drugs are being overprescribed, and given to children with minor behavioral issues. A recent story in a European newspaper about the increased use of ADHD medications, for example, was headlined “Zombie Generation.” Yet the reality is there’s very little data to tell us the degree to which these medications are being used appropriately or not.

Antipsychotic medications, such as Risperdal, Seroquel and Abilify, were developed to treat adults with major mental illnesses including schizophrenia and bipolar disorder. But in recent years, their use has extended to treat conditions such as autism and attention-deficit/hyperactivity disorder (ADHD) in children and adolescents.

How these medications work remains somewhat of a mystery, although we know they affect multiple brain neurotransmitters such as dopamine and serotonin.

Because these medications’ side effects include an increased risk for conditions such as obesity, diabetes and movement disorders, they’re subject to extra scrutiny to make sure that the right medications are being prescribed to the right patients at the right time.

For instance, the American Academy of Child and Adolescent Psychiatry has a list of 19 “best practice” recommendations. These include using just one medication at a time, avoiding the medications in very young children, monitoring for side effects, and trying other treatments first for things like ADHD and aggressive behavior.

Are doctors following prescribing guidelines?

With the rise in antipsychotic medication prescriptions, we wanted to know how well doctors were following these recommendations.

As a member of the Vermont Psychiatric Medications for Children and Adolescents Trend Monitoring workgroup, we were tasked with offering recommendations to our state legislature and other government agencies about psychiatric medication use in youth. We knew antipsychotic prescribing rates in Vermont had been somewhat high, but had dropped in recent years relative to other states. Without digging deeper, we couldn’t actually tell what this trend meant.

To learn more about why and when these medications are prescribed, we sent a survey to every provider who had prescribed an antipsychotic medication to a child covered by Medicaid in Vermont. We focused on Medicaid because we did not have access to commercial insurance databases.

Our survey was required in order for the prescription to be refilled, which meant our return rate (80%) was much higher that it would have been for a truly voluntary survey.

Clinicians aren’t always following guidelines

To our knowledge the study, which was recently published in Pediatrics, is the first one to compare antispychotic prescribing patterns to best practice guidelines.

We found evidence that these medications aren’t being doled out to treat minor behavioral problems, which is reassuring. But we also found places where doctors weren’t following best practice guidelines.

Perhaps the biggest finding was that an antipsychotic prescription followed best practice guidelines only about half the time. We also found that these medications were prescribed for an FDA-approved use only a quarter of the time.

By itself, this is bad news and means that there needs to be a greater effort to make sure these medications are being prescribed appropriately. Increasing access to child therapists who do evidence-based psychotherapy could help. So would making it easier for medical records to follow patients, particularly for kids in foster care who often move from place to place.

Antipsychotic drugs aren’t being used to treat minor behavioral issues.
Children playing via

It turns out that most providers who prescribe antipsychotic medications are not psychiatrists. About half are primary care clinicians such as pediatricians or family physicians. And 42% of the time the doctor who is responsible for maintaining the antipsychotic medication isn’t the one who originally prescribed it. This can be a problem because a doctor may be less comfortable stopping a medication that someone else started. He or she also may not know the whole story behind why the child was prescribed the medication in the first place.

The most common reason by far that prescriptions failed to meet best practice standards was because the patient was not getting the recommended lab work – for instance, monitoring blood glucose to check for early diabetes. This is a problem, but there are other ways to monitor for potential side effects of these medications. And new electronic medical records may make it easier to remind doctors when these kinds of tests should be ordered.

Using antipsychotic drugs to treat bad behavior isn’t the norm

While some of the study’s results are discouraging, there is also good news. For example, using antipsychotic medications for relatively minor behavior problems – like temper tantrums in young kids – was relatively uncommon.

Further, over 90% of the time antipsychotic medications were being used only when other types of interventions, including different medications or psychotherapy, had failed. However, in many cases the type of psychotherapy tried first was not of a type that’s been shown to be most effective in treating the child’s particular problem.

And in cases when the patient was diagnosed with a condition that antipsychotic medications are not officially approved to treat, such as physical aggression, the behavior targeted was often something with scientific evidence to support using antipsychotic medication.

In our view, these medications do indeed have a place in treatment. But too many are getting to that place too quickly and without the appropriate level of monitoring. Our hope is that Vermont and other states will keep studying this issue and support doctors, patients and families to ensure that these medications are being used appropriately and safely.

The Conversation

This article was originally published on The Conversation.
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Happy 50th anniversary to cisplatin, the drug that changed cancer treatment

This year marks the 50th anniversary of cisplatin’s accidental discovery as an anti-cancer drug. Despite its horrible side effects, and the ability of cancers to become resistant to it, the drug remains as relevant now as it was when it first reached the market.

And the good news is that the drug can, and is, being made better. New formulations are being designed to make it more effective and less toxic.

The history of cisplatin

The history of cisplatin starts not in 1965, but in 1844, when it was first created by Italian chemist Michele Peyrone. For a long time it was known as Peyrone’s chloride. But the really important event was its accidental discovery as a cancer treatment by Barnett Rosenberg, a biophysical chemist.

At the time, Rosenberg was trying to study the effect electric fields had on bacterial growth. During his experiments, he found bacteria grew 300 times their normal size, a very unusual result, when he used platinum electrodes to generate the electric fields. It took a while to figure out what was going on, but in the end he discovered the platinum electrodes were corroding in the test solution, producing cisplatin.

Rosenberg published his remarkable findings in the journal Nature and followed this up three years later with another paper showing cisplatin could cure tumours in mice.

Cisplatin has been used as a treatment for cancer since its approval by the US Food and Drug Administration in 1978. And while five other platinum drugs based on the structure of cisplatin have been developed since, it has never been replaced.

Platinum drugs are now used in 40% of all chemotherapy treatments. This has completely changed how some cancers are treated. For instance, before cisplatin’s discovery the cure rate of testicular cancer was just 10%, but when combined with early detection the cure rate is now approaching 100%.

The good and the bad

Cisplatin has to be given as an intravenous injection because it’s not effective when delivered orally. Once in the veins, it moves from the blood stream into cancer cells where it bonds with water to form a more reactive form of the drug.

In this form, the drug can stop DNA from replicating and from acting as a blueprint for making proteins. This causes cancer cells to recognise something is wrong and initiate a type of cell suicide called apoptosis.

But cisplatin is not without its problems. Its suite of horrible side effects includes severe nausea and vomiting. These two side effects are, in fact, so bad that the drug’s development was almost stopped when it was first tested on people. It was only the invention of effective anti-nausea drugs that led to cisplatin’s approval by drug authorities.

Cisplatin also makes patients anaemic and susceptible to infections. It destroys their kidneys too, although giving the patient lots of water before and after treatment has been found to be effective in reducing this.

Worse still, because these side effects are so severe, they limit the dose of the drug that can be given to patients. Many cancers end up getting treated with less than optimal doses as a result, which leads to tumours rapidly developing resistance to further treatment. This is a particular problem in the treatment of ovarian cancer because it develops resistance faster than other types of cancer.

The future of cisplatin

But there’s good news on this front. Over the last two decades, many researchers, including my research team, have been developing new formulations of cisplatin in an effort to reduce its side effects. The best way to do this is through the use of nanoparticles to better target cisplatin to cancer cells. Better targeting cancer drugs is important so they don’t attack non-cancerous tissue.

One such nanoparticle formulation being commercially developed is Lipoplatin. This formulation encloses cisplatin in a shell called a liposome, which is similar in structure to the walls of human cells. As a result, it floats in the bloodstream for longer and gets trapped selectively in tumours but not normal tissue.

And it doesn’t stop there. Novel nanoparticle formulations of cisplatin using exotic materials are also being developed, although these are much further away from being ready for human testing. To date, cisplatin has been attached to carbon nanotubes, gold nanoparticles and even spaghetti ball-like polymers called dendrimers.

My team has also attached cisplatin to the outside of nanoparticles made of rust. Because rust contains iron, we could control the movement of the nanoparticles with magnets, ensuring the drug only goes to the sites in the body where it’s needed.

This drug has revolutionised the treatment of many types of cancer, especially testicular, and remains as critically important now as when it was first discovered. So happy 50th anniversary to cisplatin and good luck to all those working to make it better.

The Conversation

This article was originally published on The Conversation.
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Anti-Aging Studies Reveal Longer Lives on the Horizon


At this very moment, there is a mouse who although appears a bit dogged and raggedy is actually quite animated and bears a wild spirit as he sniffs, scrambles, and snoops about his cage at the University of Texas Health Science Center at San Antonio. Though next to his younger siblings he appears on the runtier end of the litter, unlike them he boasts a coat of black fur lustrous enough to land him a spot on a Pantene commercial. Our said mouse’s name is Mouse UT2598 and he is 3 years old, which translates into the centennial years when it comes to a human life span, as mice typically live to around 4 years old, if they are lucky.

For the sake of this article, let’s call this mouse Mighty. So, what gives Mighty his punk-ass edge? It’s called rapamycin, a compound which is gradually revealing to scientists its ability to slow the aging process along with the havoc it can cause on certain cells. Mighty’s heart and liver are functioning as if he were an adolescent, and his tendons are far more resilient with the elasticity of a 3 year-old mouse. Evidence also reveals that his organs are damaged markedly less than is considered standard at his age, leading to the theory that Mighty may be spared the effects of cancer for quite some time longer than mice not involved in the experiments taking place at the University of Texas. In fact, place him in a line-up alongside other mice his age and the distinctions are absolutely extraordinary.

The experiment involving Mighty and rapamycin is just one of many when it comes to investigation into the aging process. Research all over the globe entails experiments with a plethora of agents, not just rapamycin, some of which are already being used to treat a number of human conditions. Scientists are assembling the puzzle by employing tactics like manipulating genes, too. Essentially, they are all in a race for the big cheese: finding ways to extend longevity and ultimately trap the aging process and curb – if not cure (or even reverse) – it altogether.

As it stands, aging is the single most potent ingredient when it comes to recipes needed for age-related diseases that eventually shorten our lives like cancer, heart conditions, Alzheimer’s and other degenerative brain ailments, and others. While the main components typically associated with heart disease are high cholesterol, obesity and high blood pressure, simply celebrating an 80th birthday can be the factor that tips the scale towards contracting a fatal heart condition – even if that 80 year-old resisted a single nibble of his birthday cake. That being said, scientists are beginning to treat aging as a disease in and of itself, one which may be sensitive to treatment as simple as a doctor’s prescription.

Let’s get back to Mighty and his happy pill. Rapamycin has its origin in dirt. That is, soil samples which were collected in 1964 on a voyage to Easter Island eventually became the foundation for developing the antibiotic, and researchers have found that mice who were given the drug were prone to longer lives (about 20% longer) than mice who did not ingest the medication. What makes rapamycin particularly interesting is that it functions in a variety of species including yeast, worms and flies – and it works even when started late in life. Thus, if studies involving the drug are successful and actually lead to human treatment, it could potentially offer benefits to those starting it in their 60s or even 80s.


Rapamycin essentially hinders the operation of a gene that both people and mice possess. It is a gene called mTOR which gives the “Okay To Go” to cells for absorbing and expending energy. In the case that there is an abundance of cell-chow, mTOR gets busy directing cells to take in nutrients and start growing. When food is in short supply, the gene retracts as a turtle would into its shell until the next opportunity to feast arises. Scientists have discovered that when cells are active and “eating”, they age substantially, chiefly due to the fact that they are working their cell-butts off to process food while belching out toxic free radicals at the same time. Thus, the mission is to metaphorically slip that cell a “mickey” and keep it mellowed out without putting it at risk of starving itself – and that’s just what rapamycin is allegedly capable of doing. But – and there’s always a but when it comes to this sort of thing – rapamycin is far from being the long-searched-for fountain of youth. In studies like that starring our friend Mighty, rapamycin has resulted in a body that is 30% smaller than average while mTor-manipulated mice developed cataracts and proved more susceptible to diabetes. The study also showed that males are inclined to progressively lose testicular functioning – not exactly a perk when it comes to a pill that may help you live longer.

Another disadvantage of rapamycin was revealed when humans who were administered the drug after kidney transplants in order to decrease the risk of rejection showed signs of higher susceptibility to diabetes. Despite this, scientists feel positive when it comes to their abilities to whip up a tantalizing cocktail when it comes to adjusting doses and arriving at the ideal blend to increase the pros when it comes to longevity rather than the cons of any possible risks.


For some researchers, the passcode for achieving longevity lies in our genes, particularly when it comes to telomeres which are essentially timekeepers of a cell’s life. When a cell divides, it automatically xeroxes its chromosomes’ DNA and telomeres carry the responsibility of cueing when to halt that copying process. Every cell division triggers squiggles of DNA to essentially tie themselves into a knot at the end of a thread (or chromosome) and eventually vanish for good. Certain factors can cause telomeres to shorten cell lives at different rates (like exposure to UV light), making them a perfect target for further research regarding the scavenger hunt for anti-aging formulas.

Healthy human bodies typically maintain a perfect waltz between telomeres and telomerase (an enzyme that handles the lengthening or shortening of DNA strands) so that telomerase can lengthens telomeres just enough that an ideal amount of lost DNA can be retrieved back. But in individuals with telomere-syndrome, ailments like bone problems, liver failure and immune disorders can occur. Discovering how to tame malfunctioning telomeres can lead to correcting their misbehavior and coming up with aging-combatant formulas.

Just over a decade ago, a scientist and her collaborator, Dr. Mary Armanios and Carol Greider (the co-discoverer of telomerase) respectively, worked together in a lab at Johns Hopkins University and met a student with a blood disorder that necessitated blood transfusions on the regular. The boy was in his 20s and already had a full head of startlingly gray hair, signs of which began showing when he was only 9 years old. Curiouser and curiouser, Armanios and Greider learned that all of his paternal relatives had died at staggeringly young ages including his grandmother who died of osteoporosis in her 60s, his father who died at 59 while waiting for a liver transplant, and his aunt and uncle who both died of pneumonia in their 60s. What’s more, the boy himself had suffered from various infections that landed him in the hospital multiple times a year – and he eventually died of a staph infection at 31. It turned out that all of the family members had a severe form of telomere malfunction known as dyskeratosis congenita.

To date, Armanio feels strongly that she will learn a lot by tinkering with telomeres, including how they can be engineered to halt aging-related ailments. Similar interest lingers at Stanford University where Helen Blau and her co-researchers have splashed cells with the precise amount of genetic matter to encourage the lengthening of telomeres. In her study, cells ceased to divide indefinitely and on the contrary started to deteriorate at a normal pace, sparking hope in Blau and her team that the cells might be used for testing in the bodies of people with dyskeratosis congenita. If the cells can target the abnormally rapid growing cells entailed in the disease, they might also be used to create techniques for turning back time on normal human aging cells.


There exists promises of age-defiance in another quite odd experiment taking place at the Harvard Stem Cell Institute. There, researchers have pinned their hopes on the cousins of our friend Mighty – but in a very unusual way. To conduct their work, scientists conjoin two mice, Siamese-twin style, so that they share the same blood system. Via this most bizarre procedure, it’s been discovered that among of a pair of harnessed mice, the older one presents more new nerve-cell growth in their brains than the younger one. The elders were also brawnier, and boasted a reversal of the heart-enlargening process that typically goes hand-in-hand with aging.

The mysterious component that appears to be the cause of these findings is a protein called GD11 which is normally aplenty in young animal blood and meager in older blood. Naturally, the team at Stanford is clawing away at this amazing discovery in hopes of unearthing an answer to the question of whether or not people who live longer have higher levels of GD11, or whether people with little amounts of the protein prove more liable to develop age-related diseases like heart complication, muscle atrophy and cognitive deterioration.


At the University of California, San Francisco, another experiment is taking place under the auspices of neurobiologist Dena Dubai and involves a hormone called called klotho. Klotho received its nomenclature after the Greek fate responsible for spinning the thread of life for mortals. Klotho is known for extending the lives of animals by 30% when in increased levels. Approximately 1 in 5 humans carry enough of the protein to tack on an extra 3 or 4 years to their lives and although it is not a passport to the land of immortality, it is certainly a bigfoot-sized step towards that mystical destination.


On that note, it is important to keep in mind that most – if not all – research is not fixed on the objective of creating neverending lifetimes, rather extending healthy lives a bit longer. While toying around with components like telomeres, klotho, and GD11 offer promising results, it is not as easy as simply whipping up the perfect recipe and stocking up Rite-Aid shelves. Further manipulation of longevity genes could involve some big league moves like gene therapy and cell transplants and of course first solving all of the questions that pop up with each answer a scientist reaches. While these riddles are the culprit for bringing researchers back to the drawing board again and again, the general outlook for battling the effects of aging is remarkably upbeat. Scientists seem to bear a spirited momentum certain to bring about some serious headway in the not-too-distant future.